Toxic nephropathies are kidney injuries caused by exposure of organism to nephrotoxins. Kidney is an organ especially susceptible to nephrotoxin damage because of its special anatomical, physiological and biochemical characteristics. Risk factors for development of toxic nephropathy include older age, female sex, hypoalbuminemia, decreased glomerular filtration rate of any aetiology and numerous other metabolic and genetic factors. Drug-induced toxic nephropathies affect different nephron segments depending on the mechanism of action of a particular drug. Nonsteroidal anti-inflammatory drugs cause a decrease of prostaglandin production which leads to a decrease in GFR and excretion of water and electrolytes. Aminoglycosides damage the proximal tubule and distal tubules by a disruption of phospholipid and mitochondrial function and by oxidative stress. Cisplatin causes dose-dependent acute tubular necrosis of proximal tubule cells. Methotrexate crystallizes in acidic urine and precipitates in tubules. Calcineurine inhibitors lower renal blood flow and cause interstitial fibrosis. Lithium causes nephrogenic diabetes insipidus, acidosis and interstitial fibrosis. Radiological iodine contrasts damage the kidney by ischaemia and direct tubular toxicity. Heavy metals are an important cause of toxic nephropathy because of environmental and drinking water pollution. They damage the proximal tubule cells by a variety of mechanisms, mainly by oxidative stress and by disruption of intracellular signal pathways. Aristolochic acid causes Balkan endemic nephropathy characterised by tubulointerstitial damage and urothelial cancer. Ethanol causes electrolyte and acid-base balance disturbances because of generalized tubule dysfunction. Ethylene-glycol causes formation of calcium oxalate crystals in tubules. Halogenated hydrocarbons damage the proximal tubule via their toxic metabolites and oxidative stress. Melamine bonds to cynauric or uric acid and leads to nephrolithiasis. Nephrotoxins are numerous and diverse, and its important to think about them in clinical practice for the timely prevention and treatment of toxic nephropathy.